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Document Details

SuperiorAntigorite4686

Uploaded by SuperiorAntigorite4686

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dental pulp inflammation pathogenesis endodontics

Summary

This document explains the pathogenesis of pulp and periapical diseases, focusing on the histology and physiology of normal dental pulp. It details the role of various factors in causing inflammation, such as microbial irritants, chemical irritants, and mechanical irritants, as well as the importance of pulp-dentin complex interactions. The document also discusses the response of the pulp to different stimuli and the factors influencing the severity of the response. It's targeted at a postgraduate level.

Full Transcript

Pathogenesis of Pulp/Periapical Dz endo “within” dontic “tooth” Why does anyone need a root canal? Due to an Infection Endo Procedural Overview • Create opening in infected tooth • File to remove the infection • Use plugger to fill canals w gutta percha • Seal opening, place any other retentive meas...

Pathogenesis of Pulp/Periapical Dz endo “within” dontic “tooth” Why does anyone need a root canal? Due to an Infection Endo Procedural Overview • Create opening in infected tooth • File to remove the infection • Use plugger to fill canals w gutta percha • Seal opening, place any other retentive measures • Crown When it comes to ‘dark teeth’ and ‘fistulas’: • Dark teeth can be: o Necrotic o Stained from trauma (internal bleeding gets into the dentinal tubules) • Pts with true ‘dark lesions’ shouldn’t feel cold when pulp vitality is done o Should indicate a necrotized root o Response to pulp vitality could indicate lesion is actually a differential, OR it could be a partially necrosed tooth (multi-rooted with still vital roots) • Fistulas may not be a true fistula as much as they are pockets of infection Why cant we simply take an antibiotic and kill the bacteria? • Only place in the body where tissue is firmly encased in a hard structure • Inflammation and swelling creates pressure that damages the blood supply and nerve Pathogenesis of Pulp and Periapical Diseases Histology and Physiology of Normal Dental Pulp • The Pulp is a unique connective tissue with vascular, lymphatic, and nervous elements that originates from neural crest cells • Resides in rigid chamber of tooth wall • Contains: o Odontoblasts § Specialized cells w a secretory function § Form dentin § Interact w dental epithelium early in tooth development to initiate the formation of enamel o Fibroblasts o Undifferentiated mesenchymal cells o Collagen type I and II o Proteoglycans o Glycoproteins o Water Pulp Dentin Complex (Synergistic) • Odontoblasts line the periphery of the pulp tissue and extend into the dentin o No dentin w/o odontoblasts o Pulp requires protection from dentin and enamel • Impacts on dentin may affect the pulp, and pulpal disturbances can affect quality/quantity of dentin • The cell rich zone of the pulp has a low level of immune cells present o Can fight of some infection but should not be relied upon • It can take 2-3 yrs for the root/pulp to fully form in a tooth, and the • Pulp chamber regress as odontoblasts form more dentin to better shield the pulp from external stimuli Innervation of the Pulp 2 main fibers: • A Delta fibers (peripheral, out into tubules) o Sharp response to thermal change o Extend between the odontoblasts o Lose their myelin sheath (slows down the nerve transmission as they die) o Extend to a distance of 100 to 200 μm into the dentinal tubules • C fibers (deep in tissue) o Unmyelinated o Dull ache that affects patients with symptomatic irreversible pulpitis Irritation • Irritation response decreases with maturity due to vasculature changes • Young teeth have ample blood supply, decreases as apices close • Rxn of the pulp to irritants is dictated by the type/duration of stimulus • Classified as Living (microbial) or Non-living (Mechanical, Thermal, Chemical) It takes 48hrs for a pt to feel an Mechanical irritants • Pulp irritation increases as prep depth increases inflammatory response o Dentin permeability > when closer to pulp o Can be caused by: § Deep scaling It takes 48hrs for antibiotics to kick in § Curettage § Removal of tooth structure w/o proper cooling • Periapical tissues can be mechanically irritated o Nerves around roots of teeth are for proprioception o Inflammation in periapical tissue affects the nerves, cause pressure sensitivity o Can be caused by: § Impact injuries § Hyper-occlusion § Over-instrumentation of root canals § Root perforation, over-extension of root canal filling materials Chemical Irritants • Antibacterial agents, irrigating agents, and chemicals present in desensitizers, liners, bases and restorative materials can cause inflammatory changes due to cytotoxicity Antibacterial Agents Irrigated Agents • Silver nitrate • Alcohol • Phenol w or w/o camphor • Chloroform • Eugenol • Hydrogen Peroxide • Various acids Microbial Irritants • Most significant cause of inflammation is microbial • Even superficial carious lesions in enamel are capable of attracting inflammatory cells in the pulp. • Initial rxn of the pulp causes immune response o Causes focal accumulation of chronic inflammatory cells (macrophages, lymphocytes, plasma cells) o Tissue can remain inflamed for extended periods and can undergo eventual/rapid necrosis Microbiology of Root Canal Infections • Normal conditions -> pulp and dentin isolated from oral microorganisms by enamel, cementum • Any breach of enamel/cementum exposes the pulp to the outside environment o Increases infection risk o Risk increases more depending on depth of lesion (dentinal tubules widen closer to pulp) Caries are the most common cause of pulp exposure • Factors that dictate severity of pulp response: o Virulence of microorganisms Infections always go o Ability to circulate inflammatory fluids to avoid increased intrapulpal pressure from crown to apex o Host resistance o Lymphatic drainage o Other irritants, microorganism byproducts, products from necrosed pulp spreading from crown to root • Bacterial contamination must be present for pulpal/periapical pathoses to develop o Endo infections classified based on anatomical location (extraradicular/intraradicular) o Intraradicular infections (biofilms) considered primary cause of endo treatment failure § Microorganisms in apical root canal, apical deltas, lateral canals can cause long standing infections § Apical biofilms have access to nutrients to facilitate growth, causes extended host response and avoids healing • Goal of RCT is to remove microorganisms from root canal system o Failure of aseptic technique can introduce microorganisms into the canal o From lack of rubber dam use, leaking rubber dam, contaminated files and instruments, etc Endodontic Infections are Biofilm Infections • Biofilms are micro-colonies of bacteria that irreversibly attach to a substratum, to dentin, or to itself • Heterogenous matrix that will act as a physical barrier to antibiotics and disinfectants o Hard to remove but must be removed to achieve healing Microbes in Endodontic Infections • Primary root canal infections have multispecies populations o Facultative o Anaerobic gram positive, gram negative o Spirochetes o Yeasts o Unidentified species • Microbiome of carious dentin leads to endo infection (pulpitis and subsequent endo infections) consists of: o Lactobacilli o Gram Neg bacteria • Epstein Barr (EBV) can be assc with irreversible pulpitis, apical periodontitis • Papilloma Virus and Human Herpes Virus can be found in exudates from acute apical abscesses Microorganism Canal Infiltration • Causes of infiltration btwn appointments: o Leakage/loss of temporary filling o Cracked tooth o Tooth left open • Other causes: o Not using a rubber dam o Caries left in tooth o Delay in getting permanent restoration Survival of Pulp under Severe Inflammation Responses Based on Apex Formation Mature Apex Immature Apex • Less likely to retain vital pulp • More likely to retain a vital pulp • Less circulation due to closed apices • More collateral circulation Pulpal Diseases (1-4-24) • Inflammatory responses begin in the pulp in locations corresponding to the location where the irritant reaches it o Ex. Incipient lesions can have inflammatory responses in pulp at the end of associated dentinal tubules o Inflammatory response will spread through coronal pulp as lesion deepens until pulp is invaded § Severe inflammation will occur at this point • Inflammatory response can be reversed when lesion can be treated conservatively or can progress to irreversible (requires professional intervention) o Degree of irritant has a positive correlation with level of inflammation • Unlike other connective tissues, the dental pulp lacks collateral circulation, it is confined within rigid dentinal walls. • Therefore at a specific point in the disease process, the inflammation changes from reversible (one that would respond favorably to conservative treatment and heal) to irreversible pulpitis. • The transition of reversible to irreversible pulpitis is important to identify because it determines the optimal treatment. • Inflammatory mediators seen in assc with increased pulpal pain in pts with symptomatic irreversible pulptis o Prostaglandins If our apex is closed and we can just remove the pulp o Neuropeptides and be fine, why do we have to have a pulp? o Bradykinin o Cytokines Loss of pulp = loss of receptor nerves. o Chemokines o Matric metalloproteinases Care must be taken to ensure undetected future • Pulp nociceptors increase excretion of Substance P and CGRP decay doesn’t occur. under inflammation o Lowers pain threshold Teeth can become more brittle when nerves removed. o Increases blood vessel permeability to inflammatory cells Pulp Stones (not pathologic) • Radiographic evidence of increased mineralization causing deposits of hard dentinal tissue in pupal space o Nerves signal for more protection, causing an increased lay down of dentinal tissue in pulp space o Associated with: § Trauma Even when it looks like there is no pulp canal § Bruxism present, there is ALWAYS some degree of pulp § Caries tissue present, even if it is just 1 cell wide § Deep restorations § Cardiovascular dz § Statin meds • Not considered pathologic Resorption • Pulp can undergo internal resorptive defects • Initiated by osteoclasts or odontoclasts (not normal inhabitant of healthy pulp) o From monocytes o Mediators of bone turnover seen in PDL, alveolar bone o Expand in size to form resorptive lesion o Not commonly found in healthy pulp • Resorption (internal or external) is pathologic even w no symptoms Process of Periapical Healing • Once irritants removed: o Inflammatory response decreases o Tissue forming cells increase (fibroblasts, endothelial cells) o Resorbed bone begins to be replaced o Resorbed cementum, dentin is repaired via cellular cementum o PDL (first affected tissue) will be restored last Calcification likes to lay down over furcations of bifurcated/trifuracted roots and deep in root canals of anterior teeth in a coronal to apical direction Factors Influencing Healing • Inherent loss of host factors (impaired blood supply, leukopenia, malnutrition) • Corticosteroids • NSAID (prevent inflammation before it happens) • Systemic dz (ex. Diabetes Mellitus) Notes from Lab: • EDTA, which is used to irrigate root canals, does not dissolve tissue • Root canal sealer paste is what seals the roots off from bacteria • Gutta percha without sealer will lead to a failed RCT

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